EFFECT OF DECREASED PLASMA LOW-DENSITY-LIPOPROTEIN LEVELS ON ADRENAL AND TESTICULAR FUNCTION IN MAN

Citation
R. Arem et al., EFFECT OF DECREASED PLASMA LOW-DENSITY-LIPOPROTEIN LEVELS ON ADRENAL AND TESTICULAR FUNCTION IN MAN, Clinical biochemistry, 30(5), 1997, pp. 419-424
Citations number
28
Categorie Soggetti
Biology,"Medical Laboratory Technology
Journal title
ISSN journal
00099120
Volume
30
Issue
5
Year of publication
1997
Pages
419 - 424
Database
ISI
SICI code
0009-9120(1997)30:5<419:EODPLL>2.0.ZU;2-S
Abstract
Objective: The study assessed whether serum LDL cholesterol levels aff ect adrenal and Leydig cell function in man. Design and Methods: A 24- h continuous ACTH infusion was performed in 15 consecutive chronically ill patients. Serum cortisol and DHEA-s were measured at baseline and at 3, 6, 12, 20, and 24 h during the infusion. Fasting serum lipoprot ein levels including LDL cholesterol, HDL cholesterol as well as FSH, LH, total and free testosterone concentrations were also measured on t he baseline morning samples prior to the infusion. Results: The initia l 3 and 6 h percent rise in cortisol values during 24-h ACTH infusion were significantly diminished in patients with LDL-C values <1.55 mmol /L as compared with patients with higher LDL-C levels (127 +/- 17% (SE ) vs. 199 +/- 31% (SE); p < 0.02 and 115 +/- 17% vs. 213 +/- 32%; p < 0.02. However, the 24-h areas of cortisol under the curve were compara ble in the 2 groups. Basal and ACTH stimulated DHEA-s levels and perce nt increases tended to be lower in the low LDL-C group but the differe nces were not statistically significant. The mean total testosterone w as lower in the low LDL-C group (5.30 +/- 1.73 vs. 15.60 +/- 1.95 nmol /L; p < 0.0005). Free testosterone levels were also lower in the low L DL-C group (0.03 +/- 0.009 nmol/L vs. 0.08 +/- 0.01 nmol/L; p < 0.001) . Five of six patients with low LDL-cholesterol had low testosterone v alues, but variable LH levels. Conclusions: Our results suggest that s evere acquired LDL cholesterol insufficiency impairs slightly the init ial glucocorticoid response to ACTH stimulation but not the overall co rtisol production during sustained ACTH stimulation. It also may contr ibute to the reduction in testosterone seen in chronically ill patient s.